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Copper in Drinking Water (2000) / Chapter Skim
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3 Health Effects of Copper Deficiencies
Pages 33-50

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From page 33...
... Additional studies have demonstrated the essentiality of copper in immune function, bone formation, red- and white-blood-cell maturation, lipid metabolism, iron transport, myocardial contraction, and neurological development (ranks 1988~. TERATOGEN ESIS OF COPPER DEFICIENCY Causes of Copper Deficiency Before a discussion of the developmental effects associated with a deficit of copper, it is important to recognize the multiple ways an embryonic or fetal copper deficiency might arise.
From page 34...
... Second, a conditioned embryonic or fetal deficiency of copper might arise if the mother has an excessive low intake of copper as a consequence of an underlying disease or if disease-induced changes in maternal copper metabolism reduces the transfer of copper to the conceptus. Third, nutritional interactions can produce conditioned deficiencies.
From page 35...
... In addition to promoting injury of neuronal cells, reductions in CuZnSOD activity result in brain edema and focal cerebral ischemic injury in CuZnSOD mutant mice (Kondo et al.
From page 36...
... PAM activity can remain low even after months of copper repletion (Prohaska and Bailey 1995~. It has not been determined whether the persistence of low PAM activity in the brain after prenatal copper deficiency is due to the relatively long period of time that it takes to increase brain copper concentrations or whether it represents a more fundamental epigenetic defect.
From page 37...
... Finally, lung abnormalities are a frequent consequence of prenatal and early postnatal copper deficiency. Lungs from neonatal rabbits born to dams fed copper-deficient diets were characterized by low concentrations of copper and lysyl oxidase activity and high proportions of poorly cross
From page 38...
... Given the significant teratogenic effects that can be associated with similar drugs in experimental animals, it is reasonable to suggest that these drugs can pose a substantial risk to the conceptus if maternal dietary copper intake is Tow. A condition of severe copper deficiency can be rapidly induced in experimental animals through the use of a number of chelating drugs, including disulfiram, DPA, TETA, and DMSA (Salgo and Oster 1974; Keen et al.
From page 39...
... However, zinc-induced fetal copper deficiencies are relatively easy to produce in experimental animals, and care should be taken to monitor women who consume zinc supplements during pregnancy. The Institute of Medicine recommends that copper supplements (2 ma)
From page 40...
... The prognosis for infants with the disorder is poor and death typically occurs before 3 years of age (ranks 1988; TurnTund 1994~. Similar to the blotchy mouse, the developmental abnormalities associated with Menkes disease are thought to be the consequence of low activity of numerous cuproenzymes during embryonic and fetal development.
From page 41...
... is typically characterized by severe connective-tissue defects and neurological abnormalities, similar to those observed with severe maternal copper deficiency. The primary genetic defect in the blotchy mouse is thought to involve a mutation in a copper-transporting ATPase gene that is homologous to the Menkes gene in humans (Des et al.
From page 42...
... Data on clinical copper deficiency is to be differentiated from copper intake data, which infer a certain frequency of copper deficiency which may be higher than that which actually occurs. Clinical copper deficiency in the United States is also to be differentiated from hypotheses suggesting that low intake of copper leads to an increased risk of atherosclerosis.
From page 43...
... More rarely, copper deficiency can result from surgical removal of a large section of the small intestine, thus greatly reducing absorption of copper. The most sensitive indicator of clinical copper deficiency is the serum ceruloplasmin level.
From page 44...
... Marginal copper intake might have adverse health effects, on the vascular and immune system.
From page 45...
... 1995. Similar splicing mutations of the Menkes/mottled coppertransporting ATPase gene in occipital horn syndrome and the blotchy mouse.
From page 46...
... 1999. Antioxidant enzyme activity in human abdominal aortic aneurysmal and occlusive disease.
From page 47...
... 1997. Reduction of CuZn-superoxide dismutase activity exascerbates neuronal cell injury and edem formation after transient focal cerebral ischemia.
From page 48...
... 1995. Alterations of rat brain peptidylglycine a-amidating monooxygenase and other cuproenzyme activities following perinatal copper deficiency.
From page 49...
... 1997. In vitro copper stimulation of plasma peptidylglycine a-amidating monooxygenase in Menkes disease variant with occipital horns.
From page 50...
... affects maternal and fetal copper metabolism in Swiss mice. Toxicology 72~1~:27-40.


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